Inflammation associated with complement activation is mediated by the release of which mediator?

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Multiple Choice

Inflammation associated with complement activation is mediated by the release of which mediator?

Explanation:
When the complement system activates during inflammation, anaphylatoxins (C3a and C5a) trigger mast cells and basophils to degranulate. This releases histamine, a key mediator that increases vascular permeability and causes vasodilation, leading to redness, warmth, and swelling at the site. Serotonin is mainly stored in platelets and can influence vascular tone in some contexts, but it isn’t the primary mediator released in this complement-triggered pathway. Prostaglandins and bradykinin contribute to inflammation as well, but they’re not the immediate mediators released in response to complement activation; prostaglandins are produced later through COX pathways, and bradykinin arises from the kallikrein–kinin system. Histamine best fits the described mechanism.

When the complement system activates during inflammation, anaphylatoxins (C3a and C5a) trigger mast cells and basophils to degranulate. This releases histamine, a key mediator that increases vascular permeability and causes vasodilation, leading to redness, warmth, and swelling at the site. Serotonin is mainly stored in platelets and can influence vascular tone in some contexts, but it isn’t the primary mediator released in this complement-triggered pathway. Prostaglandins and bradykinin contribute to inflammation as well, but they’re not the immediate mediators released in response to complement activation; prostaglandins are produced later through COX pathways, and bradykinin arises from the kallikrein–kinin system. Histamine best fits the described mechanism.

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